Cat.No. : CSC-SC012672-1 Host Cell: HeLa
| Cat. No. | CSC-SC012672-1 |
| Description | This cell line is engineered to stably express human prostaglandin-endoperoxide synthase 2 (PTGS2) in HeLa cells. |
| Gene | PTGS2 |
| Gene Species | Homo sapiens (Human) |
| Host Cell | HeLa |
| Host Cell Species | Homo sapiens (Human) |
| Stability | Validated for at least 10 passages |
| Application | 1. Gene expression studies 2. Signaling pathway research 3. Drug screening and toxicology 4. Disease research |
| Quality Control | Negative for bacteria, yeast, fungi and mycoplasma. |
| Shipping | Dry ice |
| Storage | Liquid nitrogen |
| Revival | Rapidly thaw cells in a 37°C water bath. Transfer contents into a tube containing pre-warmed media. Centrifuge cells and seed into a 25 cm2 flask containing pre-warmed media. |
| Mycoplasma | Negative |
| Format | One frozen vial containing millions of cells |
| Storage | Liquid nitrogen |
| Safety Considerations |
The following safety precautions should be observed. 1. Use pipette aids to prevent ingestion and keep aerosols down to a minimum. 2. No eating, drinking or smoking while handling the stable line. 3. Wash hands after handling the stable line and before leaving the lab. 4. Decontaminate work surface with disinfectant or 70% ethanol before and after working with stable cells. 5. All waste should be considered hazardous. 6. Dispose of all liquid waste after each experiment and treat with bleach. |
| Ship | Dry ice |
A: The PTGS2 gene, also known as COX-2, codes for the cyclooxygenase-2 enzyme. This enzyme is responsible for the production of prostaglandins, which are lipid compounds involved in various physiological processes such as inflammation, pain, and fever response. The PTGS2 gene is inducible and is upregulated in response to injury, infection, and certain cytokines.
A: The PTGS2 gene influences pain perception by mediating the production of prostaglandins, which sensitize pain receptors and enhance the transmission of pain signals in the nervous system. By inhibiting the PTGS2 gene, the production of these pain-facilitating prostaglandins can be reduced, providing relief from pain.
A: Yes, targeting the PTGS2 gene has significant therapeutic implications. Nonsteroidal anti-inflammatory drugs (NSAIDs) and COX-2 inhibitors can selectively inhibit the PTGS2 gene, reducing inflammation and pain without affecting the constitutive PTGS1 gene. This targeted inhibition is useful in managing conditions such as arthritis, inflammatory bowel disease, and postoperative pain.
A: While inhibiting the PTGS2 gene can provide relief from inflammation and pain, it may also have side effects. Since prostaglandins produced by PTGS2 play a protective role in the gastrointestinal tract, inhibiting PTGS2 can increase the risk of gastrointestinal ulcers and bleeding. Additionally, prolonged inhibition of PTGS2 may interfere with the regulation of renal function and platelet aggregation.
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The production and use of the Human PTGS2 Stable Cell Line - HeLa prioritize environmental sustainability, employing eco-friendly practices in cell culture and waste management. This commitment to reducing ecological footprint aligns with responsible research and contributes to the overall sustainability of scientific exploration.
The Human PTGS2 Stable Cell Line - HeLa is globally accessible, enabling researchers around the world to obtain and utilize this valuable tool for their studies. Its worldwide availability fosters collaboration, knowledge exchange, and the advancement of research in diverse scientific disciplines.
The Human PTGS2 Stable Cell Line - HeLa undergoes thorough functional validation post-editing, confirming the desired knockout phenotype and ensuring that the cell line accurately represents the biological effects of PTGS2 deletion. This validation is crucial for reliable experimental outcomes and the establishment of the cell line as a robust model for further research.
The gene editing technology used for the Human PTGS2 Stable Cell Line - HeLa ensures high precision in targeting the PTGS2 gene, minimizing off-target effects. This specificity is essential for accurate and meaningful research, as it eliminates potential confounding factors and enables precise investigation of the gene's functions and regulatory mechanisms.
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